Institute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Währinger Gürtel 18-20, Vienna, 1090, Austria.
Virology. 2023 Jun;583:45-51. doi: 10.1016/j.virol.2023.04.003. Epub 2023 May 3.
The human rhinovirus (HRV) A2 is endocytosed by clathrin-mediated endocytosis (CME) bound to the classical LDL receptor and releases its RNA during its transport to late endosomes. Here it is shown that - presumably due to an effect on virus recycling - a low concentration of the CME inhibitor chlorpromazine present during virus internalization (30 min) did not reduce HRV-A2 infection, but strongly inhibited short-time (5 min) endocytosis of HRV-A2. Chlorpromazine had no effect on the colocalization of the ICAM-1 ligand HRV-A89 with early endosomes, excluding CME as the main endocytosis pathway of this virus. As published for HRV-A2 and HRV-A14, HRV-A89 partially colocalized with lysosome-associated membrane protein 2 and the microtubule inhibitor nocodazole did not reduce virus infection when present only during virus internalization. Together with previous work these data suggest that there are no principal differences between endocytosis pathways of ICAM-1-binding rhinoviruses in different cell types.
人鼻病毒 (HRV) A2 通过网格蛋白介导的内吞作用 (CME) 与经典 LDL 受体结合内吞，并在运输到晚期内体时释放其 RNA。这里表明， - 可能由于对病毒回收的影响 - 在病毒内化过程中存在的低浓度 CME 抑制剂氯丙嗪（30 分钟）并没有降低 HRV-A2 感染，但强烈抑制了 HRV-A2 的短期（5 分钟）内吞作用。氯丙嗪对 ICAM-1 配体 HRV-A89 与早期内体的共定位没有影响，排除了 CME 作为该病毒的主要内吞途径。正如已发表的 HRV-A2 和 HRV-A14 所述，HRV-A89 部分与溶酶体相关膜蛋白 2 共定位，并且当微管抑制剂 nocodazole 仅在病毒内化过程中存在时，不会降低病毒感染。结合以前的工作，这些数据表明不同细胞类型中 ICAM-1 结合鼻病毒的内吞途径之间没有主要差异。
